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1
Department of Hematology [J. D., H. E., M. A.] and Clinical Investigations [T. M., K. M.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030; Fred Hutchinson Cancer Research Center, Seattle, Washington 98125 [K. A. R., S. J. C.]; and Laboratory of Cell Biology, University of Torino, Torino, Italy [F. M.]
CD38 is a leukocyte differentiation antigen that has been thought to be a phenotypic marker of different subpopulations of T-and B-lymphocytes. In myeloid cells, CD38 is expressed during early stages of differentiation. Virtually no information is available on regulation and functions of CD38. Recently we reported that all-trans-retinoic acid (ATRA) is a potent and highly specific inducer of CD38 expression in human promyelocytic leukemia cells. Here we report that ATRA-induced expression of CD38 antigen in myeloid cells is mediated through retinoic acid-
receptor (RAR). ATRA failed to induce CD38 expression in a mutant subclone of the HL-60 myeloid leukemia cell line (designated HL-60R) that is relatively resistant to ATRA-induced granulocytic differentiation. Retroviral vector-mediated transduction of RA receptor (RAR) into this HL-60R subclone completely restored the sensitivity of these cells to ATRA in terms of their ability to express CD38. In contrast, CD38 expression was not inducible by ATRA in HL-60R cells, transfected with a functional RARß, RAR
, or RXR receptor. Induction of CD38 in acute promyelocytic and acute myeloblastic leukemia cells was independent of ATRA-induced cytodifferentiation. Following culture with ATRA, increased CD38 protein levels were also observed in normal CD34+ bone marrow cells, but not on normal circulating granulocytes. From these results, we conclude that CD38 is ATRA inducible in myeloid leukemia cells and normal CD34+ bone marrow cells. This effect is independent of differentiation and is mediated by RAR in HL-60 cells, suggesting a similar role for RAR in CD38 expression in other hematopoietic cells.
1 This work was supported in part by Argus Pharmaceuticals, Inc., The Woodlands, TX, and by grants from the Food and Drug Administration (FD-R-000923), from NIH (CA 55397, CA 57369, CA 16672, and CA 55164), European Economic Community Biotechnology Project (Brussels, Belgium, BI02/CT92/0269), and Target Project "Applicazioni Cliniche Ricerca Oncologica" (Consiglio Nazionale Ricerche, Rome, Italy). K. A. R. is a special fellow of the Leukemia Society of America.
2 To whom requests for reprints should be addressed, at The University of Texas M. D. Anderson Cancer Center, Department of Clinical Investigations, Box 60, 1515 Holcombe Boulevard, Houston, TX 77030.
Received 8/17/93. Accepted 1/28/94.
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